Dyck L E, Juorio A V, Boulton A A
Neurochem Res. 1982 Jun;7(6):705-16. doi: 10.1007/BF00965523.
Administration of phenelzine (100 mg/kg. i.p., 18 hr) increased rat striatal concentrations of pTA, mTA and DA by 30, 6.7 and 1.5 fold, respectively. Lesions of the medial forebrain bundle prevented these increases, permitting the conclusion that the phenelzine-induced amine increases were localized in the synaptic terminals. The release of endogenous pTA, mTA and DA from striatal slices obtained from phenelzine-treated rats was investigated, 50 mM KC1l elicited releases of pTA, mTA and DA which were significantly greater than their respective basal releases. These K+-stimulated releases were antagonized significantly by 15 mM MgCl2, suggesting that they are calcium-dependent in nature. We have concluded, therefore, that mTA and pTA, as well as DA, are released from striatal nerve terminals in vivo. The total amounts of mTA and DA, but not pTA, released in the release experiments were greater than those found in the nonincubated tissue. It appears, therefore, that the biosynthesis of mTA and DA was stimulated during the incubation of the striatal slices.
腹腔注射苯乙肼(100毫克/千克,18小时)后,大鼠纹状体中对羟基苯乙胺(pTA)、间羟基苯乙胺(mTA)和多巴胺(DA)的浓度分别增加了30倍、6.7倍和1.5倍。内侧前脑束损伤可阻止这些增加,由此可以得出结论,苯乙肼诱导的胺类增加定位于突触终末。研究了从经苯乙肼处理的大鼠获得的纹状体切片中内源性pTA、mTA和DA的释放情况,50 mM氯化钾引起的pTA、mTA和DA释放量显著高于各自的基础释放量。这些钾离子刺激的释放被15 mM氯化镁显著拮抗,表明它们本质上是钙依赖性的。因此,我们得出结论,mTA、pTA以及DA在体内从纹状体神经终末释放。释放实验中释放的mTA和DA总量(但不包括pTA)大于未孵育组织中的含量。因此,似乎在纹状体切片孵育过程中mTA和DA的生物合成受到了刺激。